A new method for tracing the spread of spontaneous electrical seizures within the brain of epileptics has been developed. The method has now been tested in several cases in whom it has been possible to check the localizations found against the operative and histological findings after therapeutic surgery by removal of part of the anterior temporal lobe on the affected side. A new facet has been added during the period since the last report in that the technique is being used to pin-point the location of maximal effect of anticonvulsants and to compare the effectiveness of agents commonly used to control seizures. To recapitulate briefly the aims behind this methodology: The patients in this series are cases of intractable partial epilepsy who, because control of their seizures by medication has failed, are candidates for therapeutic surgery by Dr. Paul H. Crandall once localization of the more abnormal tissue has been determined. Additionally they are cases in whom this decision cannot be reached by scalp electroencephalography. Since the goal is to elucidate and locate the epileptogenic tissue responsible for the patient's complaint, only spontaneous seizures are considered pertinent. Any that could be induced by electrical stimulation at some point in the brain with the search for responses or after discharges in other loci are to be avoided, for this artificially concerted bombardment may force a breakthrough of abnormal pathways. The aim is to detect the locus whose unprovoked abnormal discharge is the source that drives and and paces other structures into the development of further abnormal activity in other parts of the brain resulting eventually in an observable or experienced seizure. Added to the project during the last year has been an investigation of the site of action of certain anticonvulsant drugs in deep structures of the epileptic brain in man and specifically on those loci where the trigger zone for spread of the seizure has been located. A differentiation is being sought as to whether the drug suppresses the activity of the original trigger or whether it suppresses its axonal and transynaptic spread to other sites.